Category:MichSt14A 26

Figures 5 and 6 work together to suggest that GldM is needed to secrete the motility factors SprB and RemA. Figure 5 shows that RemA and SprB are still produced when the gene gldM is rendered nonfunctional, so GldM is not involved in their production. However, Figure 6 shows that gldM mutants are not motile, suggesting that RemA and SprB are not being secreted in the mutants, and thus GldM is involved in secreting the proteins.

Figures 5 and 6 work together to suggest that GldL is needed to secrete the motility factors SprB and RemA. Figure 5 shows that RemA and SprB are still produced when the gene gldL is rendered nonfunctional, so GldL is not involved in their production. However, Figure 6 shows that gldL mutants are not motile, suggesting that RemA and SprB are not being secreted in the mutants, and thus GldL is involved in secreting the proteins.

Figures 5 and 6 work together to suggest that GldK is needed to secrete the motility factors SprB and RemA. Figure 5 shows that RemA and SprB are still produced when the gene gldK is rendered nonfunctional, so gldK is not involved in their production. However, Figure 6 shows that gldK mutants are not motile, suggesting that RemA and SprB are not being secreted in the mutants, and thus GldK is involved in secreting the proteins.

Figure 4 shows the expression levels of 10 genes involved in iron homeostasis in both the wild type samples and amrZ mutants. In both of the iron sufficient and iron deficient mediums, the amrZ mutants displayed significantly higher levels of iron gene expression, suggesting that amrZ plays a role in suppressing these genes.

Figure 2a shows the expression levels of comC in the wild type samples and the comE mutant samples. The wild type samples only showed an increase in comC when grown in the presence of CSP, whereas comE mutants showed high expression levels of comC, even those that were not grown in the presence of CSP.